217 Sleep in heavy marijuana users after smoking differing THC doses compared to controls

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A87-A87
Author(s):  
Mohammad Sibai ◽  
Timothy Roehrs ◽  
Gail Koshor ◽  
Jelena Verkler ◽  
Leslie Lundahl

Abstract Introduction Sleep disturbances are commonly reported by chronic marijuana (MJ) users and often identified as reasons for MJ relapse and/or other drug use. In the current study we compared the sleep architecture of 12 heavy MJ users to 11 normal controls. Methods Participants in the marijuana group met DSM-V criteria for cannabis use disorder but were otherwise healthy individuals. On the first study day, individuals smoked (1330-1400 hr) 11 puffs from a cannabis cigarette (7% THC). During the next four days, under varying experimental contingencies participants smoked an average of 4.58 (±3.48) day 1, 4.92 (±3.62) day 2, 4.75 (±3.52) day 3, and 4.17 (±3.56) day 4 puffs from cannabis cigarettes (7% THC). Their sleep was recorded the first four study nights using standard polysomnography procedures at Henry Ford Sleep and Research Center Hospital, under an 8-hr fixed time in bed (2300-0700 hr). Controls (n=11) had no history of illicit drug use or medical illness and were not shift workers. Neither group reported a history of sleep-related disorders. PSG recordings were scored using Rechtschaffen and Kales standard criteria. Sleep measures included sleep efficiency (total sleep time/time in bed * 100), latency to persistent sleep, and percent of time spent in Stage 1, 2, 3/4, and rapid eye movement (REM). Results PSGs taken across all four nights of inpatient stay showed that MJ users spent significantly more time in REM sleep compared to controls (means 24.91, 24.64, 24.42, 24.13 vs 18.81, p<.001) and less time in stage 3/4 sleep (means 4.33, 4.79, 4.53, 6.91 vs 15.68, p<.001). MJ users showed reduced sleep efficiency compared to controls on night 4 (means 82.03 vs 90.32, p=0.039), and increased latency to persistent sleep on night 1 (means 6.04 vs 17.77, p=0.026). Conclusion These data show reduced sleep efficiency, lightened sleep (reduced stage 3/4), as well as an increased duration during REM sleep in heavy MJ users during decreased use, findings that are predictive of relapse in other drug abuse populations. Support (if any) NIH/NIDA R21 DA040770 (LHL)

Nutrients ◽  
2021 ◽  
Vol 13 (1) ◽  
pp. 248
Author(s):  
Michael J. Patan ◽  
David O. Kennedy ◽  
Cathrine Husberg ◽  
Svein Olaf Hustvedt ◽  
Philip C. Calder ◽  
...  

Emerging evidence suggests that adequate intake of omega-3 polyunsaturated fatty acids (n-3 PUFAs), which include docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), might be associated with better sleep quality. N-3 PUFAs, which must be acquired from dietary sources, are typically consumed at suboptimal levels in Western diets. Therefore, the current placebo-controlled, double-blind, randomized trial, investigated the effects of an oil rich in either DHA or EPA on sleep quality in healthy adults who habitually consumed low amounts of oily fish. Eighty-four participants aged 25–49 years completed the 26-week intervention trial. Compared to placebo, improvements in actigraphy sleep efficiency (p = 0.030) and latency (p = 0.026) were observed following the DHA-rich oil. However, these participants also reported feeling less energetic compared to the placebo (p = 0.041), and less rested (p = 0.017), and there was a trend towards feeling less ready to perform (p = 0.075) than those given EPA-rich oil. A trend towards improved sleep efficiency was identified in the EPA-rich group compared to placebo (p = 0.087), along with a significant decrease in both total time in bed (p = 0.032) and total sleep time (p = 0.019) compared to the DHA-rich oil. No significant effects of either treatment were identified for urinary excretion of the major melatonin metabolite 6-sulfatoxymelatonin. This study was the first to demonstrate some positive effects of dietary supplementation with n-3 PUFAs in healthy adult normal sleepers, and provides novel evidence showing the differential effects of n-3 PUFA supplements rich in either DHA or EPA. Further investigation into the mechanisms underpinning these observations including the effects of n-3 PUFAs on sleep architecture are required.


SLEEP ◽  
2021 ◽  
Author(s):  
Olivia Herrmann ◽  
Bronte Ficek ◽  
Kimberly T Webster ◽  
Constantine Frangakis ◽  
Adam P Spira ◽  
...  

Abstract Study Objectives To determine whether sleep at baseline (before therapy) predicted improvements in language following either language therapy alone or coupled with transcranial direct current stimulation (tDCS) in individuals with primary progressive aphasia (PPA). Methods Twenty-three participants with PPA (mean age 68.13 ± 6.21) received written naming/spelling therapy coupled with either anodal tDCS over the left inferior frontal gyrus (IFG) or sham condition in a crossover, sham-controlled, double-blind design (ClinicalTrials.gov identifier: NCT02606422). The outcome measure was percent of letters spelled correctly for trained and untrained words retrieved in a naming/spelling task. Given its particular importance as a sleep parameter in older adults, we calculated sleep efficiency (total sleep time/time in bed x100) based on subjective responses on the Pittsburgh Sleep Quality Index (PSQI). We grouped individuals based on a median split: high versus low sleep efficiency. Results Participants with high sleep efficiency benefited more from written naming/spelling therapy than participants with low sleep efficiency in learning therapy materials (trained words). There was no effect of sleep efficiency in generalization of therapy materials to untrained words. Among participants with high sleep efficiency, those who received tDCS benefitted more from therapy than those who received sham condition. There was no additional benefit from tDCS in participants with low sleep efficiency. Conclusion Sleep efficiency modified the effects of language therapy and tDCS on language in participants with PPA. These results suggest sleep is a determinant of neuromodulation effects. Clinical Trial: tDCS Intervention in Primary Progressive Aphasia https://clinicaltrials.gov/ct2/show/NCT02606422


2019 ◽  
Vol 35 (4) ◽  
pp. 713-724
Author(s):  
Theresa Casey ◽  
Hui Sun ◽  
Helen J. Burgess ◽  
Jennifer Crodian ◽  
Shelley Dowden ◽  
...  

Background: Metabolic and hormonal disturbances are associated with sleep disturbances and delayed onset of lactogenesis II. Research aims: The aim of this study was to measure sleep using wrist actigraphy during gestation weeks 22 and 32 to determine if sleep characteristics were associated with blood glucose, body mass index, gestational related disease, delayed onset of lactogenesis II, or work schedule. Methods: Demographic data were collected at study intake from primiparous women who wore a wrist actigraph during gestation weeks 22 ( n = 50) and 32 ( n = 44). Start and end sleep time, total nighttime sleep, sleep efficiency, wake after sleep onset, and sleep fragmentation were measured. Night to night variability was assessed with the root mean square of successive difference. Blood glucose levels, body mass index, and gestational disease data were abstracted from medical charts. Timing of lactogenesis II was determined by survey. Results: Between gestation week 22 and 32, sleep efficiency decreased and fragmentation increased ( p < .05). During gestation week 32, blood glucose was negatively correlated with sleep duration, and positively related to fragmentation ( p < .05). Women who experienced delayed lactogenesis II had lower sleep efficiency and greater fragmentation ( p < .05), and greater night-to-night variability in sleep start and end time, efficiency, and duration during gestation week 32 ( p < .05). Conclusion: Women with better sleep efficiency and more stable nightly sleep time are less likely to experience delayed onset of lactogenesis II. Interventions to improve sleep may improve maternal health and breastfeeding adequacy.


Author(s):  
Ganesh Ingole ◽  
Harpreet S. Dhillon ◽  
Bhupendra Yadav

Background: A prospective cohort study to correlate perceived sleep disturbances in depressed patients with objective changes in sleep architecture using polysomnography (PSG) before and after antidepressant therapy.Methods: Patients were recruited into the study after applying strict inclusion and exclusion criterion to rule out other comorbidities which could influence sleep. A diagnosis of Depressive episode was made based on ICD-10 DCR. Psychometry, in the form of Beck Depressive inventory (BDI) and HAMD (Hamilton depression rating scale) insomnia subscale was applied on Day 1 of admission. Patients were subjected to sleep study on Day 03 of admission with Polysomnography. Patients were started on antidepressant treatment post Polysomnography. An adequate trial of antidepressants for 08 weeks was administered and BDI score ≤09 was taken as remission. Polysomnography was repeated post remission. Statistical analysis was performed using Kruskal Wallis test and Pearson correlation coefficient.Results: The results showed positive (improvement) polysomnographic findings in terms of total sleep time, sleep efficiency, wake after sleep onset, percentage wake time and these findings were statistically significant. HAM-D Insomnia subscale was found to correlate with total sleep time, sleep efficiency, wake after sleep onset, total wake time and N2 Stage percentage.Conclusions: Antidepressant treatment effectively improves sleep architecture in Depressive disorder and HAM-D Insomnia subscale correlates with objective findings of total sleep time, sleep efficiency, wake after sleep onset, total wake time and duration of N2 stage of NREM.


Author(s):  
Aman Gul ◽  
Nassirhadjy Memtily ◽  
Pirdun Mijit ◽  
Palidan Wushuer ◽  
Ainiwaer Talifu ◽  
...  

Objective: To preliminarily investigate the clinical features and PSG in abnormal sewda-type depressive insomnia. Methods: A total of 127 abnormal sewda-type depressive insomnia patients were evaluated with overnight PSG, and 32 normal participants were compared. Results: Patients with abnormal sewda-type depressive insomnia were compared with the control group; the sleep symptoms showed a long incubation period of sleep, low sleep maintenance rate, low sleep efficiency and poor sleep quality as well as daytime dysfunction. At process and continuity of sleep: Total sleep time, sleep efficiency, sleep maintenance rate in abnormal sewda-type depressive insomnia group were shorter than the control group. Wake after sleep onset, and sleep latency were longer than the control group. At sleep structure: N1 ratio and N2 ratio in depressive insomnia group were longer than the control group, N3 ratio and REM sleep ratio shorter than the control group. At REM index: REM latency, REM cycles, and REM sleep time were shorter than the control group. Conclusion: Insomnia symptoms in abnormal sewda-type depression comorbid insomnia patients were similar to the ordinary insomnia patients. The PSG characteristics had significant changes in sleep process, sleep structure and REM indicators. The severity of the abnormal sewda-type depression was closely related to REM indicators. Change of REM sleep characteristics may be the specificity, and these could be taken as reference in diagnosis and identification of abnormal sewda-type depressive insomnia.


SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A236-A237
Author(s):  
Jodi Gustave ◽  
Kaelyn Gaza ◽  
Jennifer Marriner ◽  
Seema Rani ◽  
Abigail Strang ◽  
...  

Abstract Introduction Children with achondroplasia and Trisomy 21 (T21) have increased incidence of sleep disturbances including sleep disordered breathing. Abnormal sleep architecture has been documented in children with T21. It is important to continue to analyze sleep parameters in both groups since poor sleep quality is associated with neurocognitive impairment. Methods Following IRB approval, we performed a retrospective chart review of patients at Nemours/A.I. duPont Hospital for Children in Wilmington, DE with achondroplasia and T21 who underwent an initial polysomnogram (PSG) between 2015 and 2020. We compared sleep architecture parameters between the groups including sleep efficiency, total sleep time (TST), sleep latency, arousal index and concentration of N3 and REM sleep. Results In patients with achondroplasia (n=49, mean age 5.8 months and 63.3% male), 12% reported restless sleep. PSG data revealed TST of 392 minutes, mean sleep efficiency of 82%, mean sleep latency of 9.4 min, mean arousal index of 40, 22% REM sleep and 32% N3 sleep. In the patients with T21 (n=32, mean age 17.8 months and 50% male), 59% reported restless sleep. PSG data revealed TST of 393 minutes, mean sleep efficiency of 82%, mean sleep latency of 14 minutes, arousal index of 35, 15% REM sleep and 40% N3 sleep. The differences in REM and N3 sleep between the two groups were statistically significant (p-values of 0.001 and 0.04, respectively), but the differences in arousal index, TST and sleep efficiency were not. Conclusion Our study showed that children with T21 subjectively noted more restless sleep compared to patients with achondroplasia although TST and sleep efficiency were similar. Patients with achondroplasia had a higher arousal index that was not statistically significant. Children with achondroplasia had a shorter sleep latency and more robust REM concentration, likely due to their younger age. There was a higher concentration of N3 sleep in patients with T21. This is likely due to the decrease in REM concentration. In conclusion, it is important to establish expected sleep parameters in patients with achondroplasia and T21 to maximize sleep quality and mitigate negative neurocognitive effects of poor sleep. Support (if any):


2015 ◽  
Vol 30 (1) ◽  
pp. 89-93 ◽  
Author(s):  
C. Boudebesse ◽  
P.-A. Geoffroy ◽  
C. Henry ◽  
A. Germain ◽  
J. Scott ◽  
...  

AbstractStudy objectives:Obesity and excess bodyweight are highly prevalent in individuals with bipolar disorders (BD) and are associated with adverse consequences. Multiple factors may explain increased bodyweight in BD including side effects of psychotropic medications, and reduced physical activity. Research in the general population demonstrates that sleep disturbances may also contribute to metabolic burden. We present a cross-sectional study of the associations between body mass index (BMI) and sleep parameters in patients with BD as compared with healthy controls (HC).Methods:Twenty-six French outpatients with remitted BD and 29 HC with a similar BMI completed a 21-day study of sleep parameters using objective (actigraphy) and subjective (PSQI: Pittsburgh Sleep Quality Index) assessments.Results:In BD cases, but not in HC, higher BMI was significantly correlated with lower sleep efficiency (P = 0.009) and with several other sleep parameters: shorter total sleep time (P = 0.01), longer sleep onset latency (P = 0.05), higher fragmentation index (P = 0.008), higher inter-day variability (P = 0.05) and higher PSQI total score (P = 0.004).Conclusions:The findings suggest a link between a high BMI and several sleep disturbances in BD, including lower sleep efficiency. Physiological mechanisms in BD cases may include an exaggeration of phenomena observed in non-clinical populations. However, larger scale studies are required to clarify the links between metabolic and sleep-wake cycle disturbances in BD.


SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A312-A314
Author(s):  
Nathan Walker ◽  
Bradley Vaughn

Abstract Introduction Frontotemporal dementia (FTD) is a degenerative process and,as the name implies, involves the frontal and temporal lobes of the brain. Patients with FTD make up 10–15% of all cases of dementia and 20% diagnosed before age 65, however not much is reported about sleep disturbances in these patients. Given the area of neuronal loss one would expect that sleep may be influenced early and by issues in arousal mechanisms and in breathing pattern. This study examined the polysomnography (PSG) reports of patients with a diagnosis FTD. Methods A retrospective chart review was performed to identify patients with both a diagnosis of FTD and having undergone a PSG. 23 patients were identified as fulfilling both requirements. Data recorded included, diagnosis, age at time of PSG, Epworth sleepiness scale (ESS), total sleep time (TST), wake after sleep onset (WASO), sleep latency (SL), REM sleep latency, sleep efficiency (SE), percentage of stage N1, N2, N3, and REM sleep, apnea-hypopnea index (AHI), presence of Cheyne-Stoke breathing, periodic limb movement index, and presence of REM without atonia. Results Patient age ranged from 57–85 years. Average ESS was 8.8 with only 5 patients reported excessive daytime sleepiness(as assessed by ESS). The average TST was 290 minutes, average SL was 37.9 minutes, average WASO was 147.5 minutes, and average sleep efficiency was 60.3%. Patients spent the majority of time in N2 sleep with an average of 68.3% of the time spent in N2. The average time spent in N3 was 9.6% of sleep. 8.9% of sleep was spent in REM. 83% of patients were diagnosed with sleep apnea (as defined by an AHI &gt; 5), with an average AHI of 20.2 events/hour. Cheyne-Stokes breathing was only noted in 4 of the 23 patients, or 17%. Periodic limb movements of sleep were noted in 48% of the patients (n=11). REM without atonia or RBD was not noted for any patients. Conclusion This study shows that patients with FTD suffer from typical sleep disturbances, however there is a high prevalence of sleep apnea as well as PLMS. In addition, patients with FTD have decreased sleep efficiency with increased WASO. Support (if any):


Circulation ◽  
2017 ◽  
Vol 135 (suppl_1) ◽  
Author(s):  
David S Curtis ◽  
Thomas E Fuller-Rowell ◽  
Mona El-Sheikh ◽  
Kristen L Knutson ◽  
Kiarria N Kershaw ◽  
...  

Introduction: Approximately half of the disparity in premature mortality between African American (AA) and European American (EA) adults is due to greater hypertension, diabetes, and stroke risk. The current study tests sleep as a mediator of racial disparities in cardiometabolic (CMB) disease risk in adulthood. Methods: A total of 618 CARDIA Study members took part in a sleep sub-study (2003-2005) and had measured CMB risk (2000-2011; mean age at baseline=40.1; 43.5% AA; 56.5% EA; 42.1% male). Sleep efficiency (% of time in bed asleep) and total sleep time were assessed via actigraphy for six total nights in years 17 and 18 of the CARDIA Study. CMB risk was assessed in years 15 and 25 from borderline high (coded as 1) and high (coded as 2) levels in seven markers using recommended cutpoints from NCEP ATP III and AHA: blood pressure, glucose, insulin resistance, waist circumference, triglycerides, HDL-C, and C-reactive protein. Scores were averaged across markers, ranging from 0 to 2 (a score of 1 indicates a borderline high average in the seven markers). Using linear path models, sleep variables were tested as mediators of racial disparities in ten-year changes in CMB risk. Results: AAs obtained less efficient sleep and less total sleep than EAs (76.5% vs 84.3%; 5.63 hrs vs. 6.43 hrs), and AAs had higher CMB risk at both periods (Mean at Y15: .75 vs. .55; Y25: .94 vs. .67) ( p ’s < .001). Mediation tests are shown in the Table. Race was indirectly associated with increasing CMB risk over the ten-year period via sleep efficiency, explaining 25% of the racial disparity. Racial disparities in CMB risk were attenuated by 24.5% when adjusting for sleep time, although the mediation test was not significant. After adjusting for education and household income, 18.1% of the race disparity in diverging CMB risk was explained by sleep efficiency and 20.8% by sleep time. Conclusions: Differences in sleep likely contribute to greater CMB risk among AAs as compared to EAs in adulthood. Sleep may be an important intervention point to reduce racial health disparities.


2012 ◽  
Vol 302 (5) ◽  
pp. R533-R540 ◽  
Author(s):  
Irwin Feinberg ◽  
Nicole M. Davis ◽  
Evan de Bie ◽  
Kevin J. Grimm ◽  
Ian G. Campbell

We recorded sleep electroencephalogram longitudinally across ages 9–18 yr in subjects sleeping at home. Recordings were made twice yearly on 4 consecutive nights: 2 nights with the subjects maintaining their ongoing school-night schedules, and 2 nights with time in bed extended to 12 h. As expected, school-night total sleep time declined with age. This decline was entirely produced by decreasing non-rapid eye movement (NREM) sleep. Rapid eye movement (REM) sleep durations increased slightly but significantly. NREM and REM sleep durations also exhibited different age trajectories when sleep was extended. Both durations exceeded those on school-night schedules. However, the elevated NREM duration did not change with age, whereas REM durations increased significantly. We interpret the adolescent decline in school-night NREM duration in relation to our hypothesis that NREM sleep reverses changes produced in plastic brain systems during waking. The “substrate” produced during waking declines across adolescence, because synaptic elimination decreases the intensity (metabolic rate) of waking brain activity. Declining substrate reduces both NREM intensity (i.e., delta power) and NREM duration. The absence of a decline in REM sleep duration on school-night sleep and its age-dependent increase in extended sleep pose new challenges to understanding its physiological role. Whatever their ultimate explanation, these robust findings demonstrate that the two physiological states of human sleep respond differently to the maturational brain changes of adolescence. Understanding these differences should shed new light on both brain development and the functions of sleep.


Sign in / Sign up

Export Citation Format

Share Document